Q-omics provides the consensus-scored HPS1 profile across patient tissues and cancer cell-line models. HPS1 expression is associated with patient survival in 24 of 34 cancer types, with the highest sampling consensus in UVM. Among the 18 cancer types available for tumor–normal comparison, HPS1 is differentially expressed in 14, with the highest sampling consensus in KIRC. Additionally, HPS1 protein abundance shows 21,132 significant protein co-abundance associations, with the highest sampling consensus in LUAD. Together, these results highlight UVM, KIRC, and LUAD as cancer lineages where HPS1 shows reproducible signals across survival, tumor–normal expression, and patient cross-omics analyses.
Every result is evaluated using two consensus scores. Sampling consensus measures how consistently a finding is reproduced within a cancer lineage across different conditions. Lineage consensus measures how broadly the result is shared across cancer types, distinguishing pan-cancer signals from lineage-specific patterns.
Premium analyses for HPS1 — synthetic lethality, tumor antigen, and pembrolizumab response.
This table summarizes HPS1 survival associations across molecular data types. HPS1 RNA expression shows survival associations in the most cancer types (24), followed by mutation status (6) and mass-spec protein abundance (10). The rightmost column indicates the cancer type with the highest sampling consensus for each molecular layer.
This table ranks reproducible HPS1 RNA expression–survival associations across cancer types. High HPS1 expression shows unfavorable associations in OV, LGG and LAML, but favorable associations in UVM, UCEC and CESC. The UVM Kaplan–Meier curve shows clear separation, with the low-expression group declining faster, consistent with the favorable association (log-rank p = .001). Together, the overview and detailed table identify UVM as the clearest survival context for HPS1 RNA expression.
This table summarizes HPS1 tumor–normal expression differences by data type. RNA shows broader differences across cancer types, with a lineage consensus of 14, while mass-spec protein shows differences in 9. The strongest signals are observed in KIRC for RNA and LSCC for protein.
This table ranks reproducible tumor–normal expression differences for HPS1. A negative fold-change indicates higher expression in normal tissue than in tumor tissue. HPS1 shows lower tumor expression in KICH and LUAD and higher tumor expression in KIRC, HNSC, LIHC and KIRP. The KIRC box plot shows higher HPS1 RNA expression in tumor versus normal tissue (log2 FC = +0.571, t-test p < 0.001).
This table shows molecular features associated with HPS1 in patient tissues and cancer cell lines. In patient samples, HPS1 shows the broadest associations at the RNA and protein expression levels, with LUAD recurring as the lineage with the largest associated feature set. In cancer cell lines, HPS1 RNA and mutation anchors are most strongly linked to RNA-expression features, especially in LUNG_NSCLC_LUAD, while CRISPR and shRNA rows add functional-dependency signals in STOMACH and BLOOD_Lymphoma.
